RESUMEN
Subsets of lymphocytes infiltrating the gastric mucosa were phenotyped by their surface antigens in biopsies of 30 patients with chronic gastritis (12 with superficial, 9 with atrophic gastritis and 9 with gastric atrophy) and 10 controls. Using direct and indirect immunofluorescent staining, monoclonal antibodies OKT3, OKT4, OKT8, OKB7, antiLeu11b and anti-IL-2 receptor were employed to detect T cell subsets, B cells, NK cells and activated cells. Most of the infiltrating lymphocytes were T cells expressing the CD4 phenotype. B cell proportions were found to increase in relation to the severity of the gastric lesion. IL-2 receptor positive cells were significantly increased in superficial gastritis. These findings indicate an involvement of T cells in the pathogenesis of chronic gastritis. Furthermore, the predominance of CD4 positive cells together with the increase of B cells parallel to the severity of the gastric lesion possibly support the concept of a T-B cooperation leading to tissue damage.
Asunto(s)
Antígenos de Diferenciación/análisis , Gastritis/patología , Linfocitos/patología , Linfocitos T Colaboradores-Inductores/patología , Adulto , Enfermedades Autoinmunes/inmunología , Enfermedades Autoinmunes/patología , Linfocitos B/patología , Recuento de Células , Femenino , Gastritis Atrófica/patología , Humanos , Cooperación Linfocítica , Linfocitos/inmunología , Masculino , Persona de Mediana Edad , Linfocitos T Colaboradores-Inductores/inmunologíaRESUMEN
1. We have studied the plasma lipoprotein abnormalities in obstructive jaundice to test the hypothesis that the abnormalities would correlate with plasma lecithin--cholesterol acyltransferase activity. 2. Very-low-density lipoproteins (VLDL) were normal in composition and had a normal pre-beta electrophoretic mobility when lecithin--cholesterol acyltransferase activity was high. When it was low VLDL had abnormal composition and ran in the beta position. 3. With high lecithin--cholesterol acyltransferase activity, low-density lipoprotein (LDL) was normal and cholestatic LDL (LP-X) was not found. With low lecithin--cholesterol acyltransferase activity up to three LDL fractions were found: (i) large triglyceride-rich particles, (ii) LP-X and (iii) a triglyceride-rich cholesteryl ester-poor particle of normal dimensions. 4. High-density lipoprotein (HDL) concentrations correlated with lecithin--cholesterol acyltransferase activity and HDL were normal in composition and electron-microscopic appearance when the activity was high. When lecithin--cholesterol acyltransferase activity was low HDL was abnormal in composition and 'stacked discs' were seen on electron microscopy as well as normal spherical particles. 5. These results suggest that low lecithin-cholesterol acyltransferase activity may cause at least some of the lipoprotein changes of obstructive jaundice.